System and method for breaking reentry circuits by cooling cardiac tissue

ABSTRACT

Systems and methods to inhibit the conduction of certain spurious electrical impulses in the heart. Inhibition of spurious electrical impulses in the heart is accomplished by cooling one or more targeted portions of the heart. Optionally, inhibition of spurious electrical impulses may be accomplished by cooling of cardiac tissue in combination with pacing of the heart.

CROSS REFERENCE TO RELATED APPLICATIONS

This application is a continuation of U.S. patent application Ser. No.10/754,887 filed Jan. 10, 2004, now U.S. Pat. No. 7,203,537, which is acontinuation-in-part of U.S. patent application Ser. No. 09/929,478filed Aug. 14, 2001, now U.S. Pat. No. 6,895,274 and acontinuation-in-part of U.S. Ser. No. 09/231,570 filed Jan. 14, 1999,now U.S. Pat. No. 6,295,470 and a continuation-in-part of U.S. patentapplication Ser. No. 10/053,750 filed Jan. 21, 2002, which is acontinuation of U.S. patent application Ser. No. 09/690,947, filed Oct.18, 2000, now U.S. Pat. No. 6,341,235. The 10/754,887 application claimspriority under 35 U.S.C. §119(e) from provisional application No.60/439,206 filed Jan. 10, 2003. The Ser. Nos. 09/929,478, 10/053,750,10/754,887, and 60/387,517 applications, as well as the U.S. Pat. Nos.6,295,470, 6,341,235, and 6,895,274, are all incorporated by referenceherein, in their entireties, for all purposes.

INTRODUCTION

The present invention relates generally to a system and method for thestimulation of cardiac muscle tissue. In particular, the embodiments ofthe present invention provide a system and method for treating cardiactissue by cooling the cardiac tissue to inhibit the conduction ofcertain electrical signals in cardiac tissue and decrease the durationof tachycardia and enhance the effects of pacing and defibrillationstimuli.

BACKGROUND

The function of the cardiovascular system is vital for survival. Throughblood circulation, body tissues obtain necessary nutrients and oxygen,and discard waste substances. In the absence of circulation, cells beginto undergo irreversible changes that lead to death. The muscularcontractions of the heart are the driving force behind circulation.

Each of the heart's contractions, or heartbeats, is triggered byelectrical impulses. These electrical impulses are sent from thesinoatrial node (the heart's natural pacemaker), which is located at thetop of the upper-right chamber of the heart or right atrium. From there,the electrical impulses travel through the upper chambers of the heart(atria) and to the atrioventricular (AV) node, where they aretransmitted to the lower chambers of the heart ventricles via the“bundle branches.” Thus, the electrical impulses travel from thesinoatrial node to the ventricles, to trigger and regulate theheartbeat.

An arrhythmia is an abnormal heartbeat resulting from any change,deviation or malfunction in the heart's conduction system—the systemthrough which normal electrical impulses travel through the heart. Undernormal conditions, each of the heart's contractions, or heartbeats, istriggered by electrical impulses. These electrical impulses are sentfrom the sinoatrial node (the heart's natural pacemaker), which islocated at the top of the upper-right chamber of the heart or rightatrium. From there, the electrical impulses travel through the upperchambers of the heart (atria) and to the atrioventricular (AV) node,where they are transmitted to the lower chambers of the heart ventriclesvia the “bundle branches.” Thus, the electrical impulses travel from thesinoatrial node to the ventricles, to trigger and regulate theheartbeat.

When the electrical “circuits” of the heart do not operate optimally, anarrhythmia may result. An arrhythmia may result in unusually fast(tachycardia) or unusually slow (bradycardia) heartbeats. The cause ofan arrhythmia may be related to a previous heart condition (e.g.,previous damage from a heart attack) or to other factors (e.g., drugs,stress, not getting enough sleep). In the majority of cases, a skippedbeat is not medically significant. The most serious arrhythmias,however, contribute to approximately 500,000 deaths in the United Stateseach year according to the American Heart Association. Sudden cardiacdeath (“cardiac arrest”) is responsible for approximately one-half ofall deaths due to heart disease, and is the number one cause of death inthe US, according to the North American Society of Pacing andElectrophysiology.

Almost all clinically important tachyarrhythmias are the result of apropagating impulse that does not die out but continues to propagate andreactivate cardiac tissue (referred to as “reentry”). Suchtachyarrhythmias include sinus node reentry, atrial fibrillation, atrialflutter, atrial tychycardia, AV nodal reentry tachycardia, AV reentry(Wolff-Parkinson-White syndrome or concealed accessory AV connection),ventricular tachycardia, and bundled branch reentrant tachycardia.

For reentry to occur, there must exist a substrate in the cardiac tissuecapable of supporting reentry (the “reentry circuit”). The activationwave front must be able to circulate around a central area of block andencounter a unidirectional block such that it is forced to travel in onedirection around the central block. (If the activation wave front ispermitted to travel in both directions around the block, the wave frontswill collide and die out.) Of importance is the conductance speed of thecirculating wave front. If the conductance speed is too fast, thecirculating wave front will arrive at its point of origin before thetissue has repolarized sufficiently to become excitable again. Thus, atleast one area of slow conductance is part of the reentry circuit forvirtually all clinical reentrant rhythms. Eliminating the slowconductance elements of a reentry circuit destroys the circuit.

Atrial fibrillation (AF) is the most common type of sustainedarrhythmia, affecting two million people each year in the United Statesalone. Both atrial fibrillation and atrial flutter increase the risk ofstroke. According to the American Heart Association, they lead to over54,000 deaths in the United States each year. The risk of developingatrial fibrillation increases dramatically with age. As a result,approximately 70 percent of patients with atrial fibrillation arebetween the ages of 65 and 85 years old. AF is a rapid, abnormal heartrhythm (arrhythmia) caused by faulty electrical signals from the upperchambers of the heart (atria). Electrical signals should normally becoming only from the sinoatrial node in a steady rhythm—about 60 to 100beats per minute. A heart experiencing AF presents two heart rates—anatrial rate and a heart rate. With AF, the atrial rate is 300-400 beatsper minute while the heart rate is 100-175 beats per minute. This heartrate is the result of the AV node blocking out most of the atrialimpulses, and allowing only the fewer impulses to emerge to theventricle.

Certain arrhythmias are related to specific electrical problems withinthe heart. AV nodal reentrant tachycardia is an arrhythmia caused by anextra conducting pathway within the AV node. This allows the heart'selectrical activity to “short circuit” or recycle within the AV nodalregion.

AV reentrant tachycardia results from an extra conducting pathway thatallows the electrical impulse to “short circuit” and bypass the AV nodealtogether. In this mode, the extra “circuit” directly links the atriaand ventricles. In most cases, this pathway can only conduct“backwards”—from ventricles to atria. This is called a “concealedaccessory pathway” since it cannot be diagnosed from a regularelectrocardiogram (EKG). These arrhythmias may be treated medically, butcan also be cured by catheter ablation. Less often, the extra pathwayconducts in the forward direction (from atrium to ventricle) and isevident on the EKG, in which case the condition is called theWolff-Parkinson-White syndrome (WPW). WPW syndrome may result inextremely rapid heartbeats and could potentially result in death.Symptomatic WPW syndrome generally requires catheter ablation.

A quite different (and life threatening) condition is ventricularfibrillation. Ventricular fibrillation involves a quivering of theventricles instead of the atria. Unlike AF, it is life threateningbecause it results in 350 beats per minute or higher. The heart cannotkeep that rate up for more than a few minutes without treatment (e.g.,with a defibrillator).

Under some conditions, arrhythmias may be transient. For example, apatient may be experiencing a particular period of stress, an illness,or a drug (legal or otherwise) reaction. In other cases, more invasivetreatments are helpful. For a slow heartbeat (bradycardia), the mostcommon treatment is an electronic (artificial) pacemaker. This device,which is implanted under the skin and permanently attached to the heart,delivers an electrical impulse when a slowing or irregularity of theheart rhythm is detected. For abnormally fast heartbeat rates, animplantable cardioverter defibrillator (ICD) may be implanted. An ICDmonitors and, if necessary, corrects an abnormally fast heartbeat. Thesedevices may be lifesaving for patients with ventricular fibrillation orventricular tachycardia. Another procedure is an electrophysiology studywith catheter ablation. This is a procedure in which catheters areintroduced into the heart from blood vessels in the legs and/or neck andradio frequency energy is used to very carefully destroy (ablate) theabnormal areas of the heart that are creating the arrhythmias.

In cardiac muscle, the muscle fibers are interconnected in branchingnetworks that spread in all directions through the heart. When anyportion of this net is stimulated, a depolarization wave passes to allof its parts and the entire structure contracts as a unit. Before amuscle fiber can be stimulated to contract, its membrane must bepolarized. A muscle fiber generally remains polarized until it isstimulated by some change in its environment. A membrane can bestimulated electrically, chemically, mechanically or by temperaturechange. The minimal stimulation strength needed to elicit a contractionis known as the threshold stimulus. The maximum stimulation amplitudethat may be administered without eliciting a contraction is the maximumsubthreshold amplitude.

Throughout much of the heart are clumps and strands of specializedcardiac muscle tissue. This tissue comprises the cardiac conductionsystem and serves to initiate and distribute depolarization wavesthroughout the myocardium. Any interference or block in cardiac impulseconduction may cause an arrhythmia or marked change in the rate orrhythm of the heart.

Biphasic—either cathodal or anodal—current may be used to stimulate themyocardium. However, until the work embodied in U.S. Pat. Nos. 5,871,506and 6,141,586 for example, anodal current was thought not to be usefulclinically. Cathodal current comprises electrical pulses of negativepolarity. This type of current depolarizes the cell membrane bydischarging the membrane capacitor, and directly reduces the membranepotential toward threshold level. Cathodal current, by directly reducingthe resting membrane potential toward threshold has a one-half toone-third lower threshold current in late diastole than does anodalcurrent. Anodal current comprises electrical pulses of positivepolarity. Presently, virtually all artificial pacemaking is done usingstimulating pulses of negative polarity although the utility of anodalpulse has been demonstrated.

The typical implantable cardioverter/defibrillator (ICD) delivers aninitial electrical countershock within ten to twenty seconds ofarrhythmia onset, thereby saving countless lives. Improved devices haveantitachycardia pacing capabilities in addition tocardioverting/defibrillating functions. These ICDs are capable ofdifferent initial responses to one or more tachycardia as well as aprogrammable sequence of responses to a particular arrhythmia.

The output energy level is generally set by a physician in accordancewith a patient's capture threshold, determined at the time of heartimplantation. This threshold represents the minimum pacing energyrequired to reliably stimulate a patient's heart. However, due to traumaassociated with the stimulation, scar tissue grows at the interfacebetween the implanted cardiac pacer leads and the myocardium. This scartissue boosts the patient's capture threshold. To insure reliablecardiac capture, the output energy level is thus generally set at alevel which is a minimum of two times greater than the initiallymeasured capture threshold. A drawback to such an approach is that thehigher stimulation level causes more trauma to the cardiac tissue thanwould a lower level of stimulation, and hence promotes the formation ofscar tissue, thereby boosting the capture threshold. The higherstimulation level also shortens battery life. This is not desirable, asa shorter battery life necessitates more frequent surgery to implantfresh batteries.

Another drawback is the potential for patient discomfort associated withthis higher stimulation level. This is because the higher stimulationlevel can stimulate the phrenic or diaphragmatic plexus or causeintercostal muscle pacing. Lastly, the higher stimulation is lesseffective, due to entry block.

Improvements to pacing technology have resulted in an enhancedconduction of electrical pulses associated with resultant heartbeats forthose arrhythmia victims who do not respond to ordinary pacing. Forexample U.S. Pat. No. 6,343,232 B1 entitled “Augmentation of MuscleContractility by Biphasic Stimulation” was issued to Morton M. Mower,M.D. That invention described increasing electrical conduction andcontractility by biphasic pacing comprising an initial anodal pulsefollowed by a cathodal pulse. This technique increased the speed ofconduction of the resultant beats by almost 100% over that produced byconventional pacing stimuli. However, this technique did not result inreversion to a sinus rhythm for all victims of cardiac conductiondisorder.

What would be truly useful is to provide alternative methods ofstimulating the myocardium and to inhibit the conduction of certainspurious electrical impulses in the heart as a substitution for, or asan enhancement to, conventional pacing and pharmaceutical therapiesand/or to use the alternative method in conjunction with conventionalpacing and safe pharmaceuticals to provide yet another method forovercoming cardiac conduction problems.

SUMMARY

An embodiment of the present invention comprises an implantable cardiactreatment/stimulation device designed to inhibit the conduction ofcertain spurious electrical impulses preferably without pacing. Thetechnique applied in the implantable device comprises a cooling elementfor cooling cardiac tissue. Optionally, the cooling process may beprovided in combination with biphasic stimulation of the cardiac tissue.

It is therefore an aspect of the present invention to inhibit theconduction of certain spurious electrical impulses in cardiac tissueaffected by re-entry circuits.

It is a further aspect of the present invention to inhibit theconduction of certain spurious electrical impulses in the heart bycooling cardiac tissue affected by re-entry circuits.

It is a further aspect of the present invention to selectively applycold temperature to areas of the cardiac tissue to inhibit theconduction of certain spurious electrical impulses in cardiac tissueaffected by re-entry circuits.

It is yet another aspect of the present invention to apply cold overlarge areas of the cardiac tissue to inhibit the conduction of certainspurious electrical impulses in cardiac tissue affected by re-entrycircuits.

It is still another aspect of the present invention to affect reentrycircuits in a more effective manner than conventional cardiac pacing.

It is still another aspect of the present invention to inhibit theconduction of certain spurious electrical impulses in the heart overlarge areas of tissue rather than only over small areas of a pacingsite.

It is a further aspect of the present invention to provide animplantable stimulation device for automatically applying cold tocardiac tissue affected by re-entry circuits.

It is yet another aspect of the present invention to provide a removabledevice for applying cold to cardiac tissue in operating room settings ortrauma settings.

It is still another aspect of the present invention to provide animplantable device that combines cooling of cardiac tissue withstimulation of cardiac tissue through conventional pacing means.

It is another aspect of the present invention to provide an implantabledevice that combines cooling of cardiac tissue with stimulation ofcardiac tissue through biphasic stimulation.

It is a further aspect of the present invention to provide animplantable cardiac stimulation device that can sense the onset offibrillation or other tachyarrhythmias and can selectively apply coolingof cardiac tissue, pacing of cardiac tissue, defibrillation of cardiactissue or a combination thereof as the situation dictates.

In one aspect of the invention, both cooling and biphasic electricalstimulation is administered to the cardiac muscle. The anodalstimulation component of biphasic electrical stimulation augmentscardiac contractility by hyperpolarizing the tissue prior to excitation,leading to faster impulse conduction, more intracellular calciumrelease, and the resulting superior cardiac contraction. The cathodalstimulation component eliminates the drawbacks of anodal stimulationalone, resulting in effective cardiac stimulation at a lower voltagelevel than would be required with anodal stimulation alone. This inturn, extends pacemaker battery life and reduces tissue damage.

In a second aspect of the invention, cooling is applied to the cardiactissue and biphasic electrical stimulation is administered to thecardiac blood pool, that is, the blood entering and surrounding theheart. This enables cardiac stimulation without the necessity of placingelectrical leads in intimate contact with cardiac tissue, therebydiminishing the likelihood of damage to this tissue. The stimulationthreshold of biphasic stimulation administered via the blood pool is inthe same range as standard stimuli delivered directly to the heartmuscle. Through the use of biphasic electrical stimulation to thecardiac blood pool, it is therefore possible to achieve enhanced cardiaccontraction, without skeletal muscle contraction, cardiac muscle damageor adverse effects to the blood pool.

Yet another embodiment of the present invention comprises an implantabledevice for automatic treatment of frequently recurring bouts of atrialfibrillation or chronic atrial fibrillation. This embodiment comprises asensing system which monitors various parameters such as the PDF(probability density function) of the atrium to sense atrialfibrillation. By sensing the PDF of the atrium, this provides a detectorfor atrial fibrillation that has not been previously considered. Uponsensing the PDF of the atrium and determining that atrial fibrillationis occurring, the implantable device of the present invention initiallyapplies cooling to the cardiac tissue of the atria. This cooling isapplied across a broad area via a contact device dimensioned to cover anextensive area of cardiac tissue. The cold temperature is then appliedover the contact device to the cardiac tissue, cooling the cardiactissue, and thereby inhibiting the conduction of spurious signalsthrough the tissue. This decreased temperature will affect the reentrycircuits in an effective fashion. Since the intervention is applied to alarge area of tissue rather than a small pacing site, the inhibition ofspurious signals can be achieved over a much broader area than a singlepoint of contact as in conventional pacing.

Cold is applied to the cardiac tissue for a brief period of time that isprogrammable and adjustable as sensors detect the need for theapplication of the cold. The amount of cooling applied and the totaltemperature of the heart are monitored through a thermostat function ofthe apparatus. Cooling can be accomplished by a mechanical hydraulicsystem for pumping cooled fluid into a bladder on the surface of theatrium.

The heart rhythm is monitored and the application of cold temperature isrepeated a number of times if initially unsuccessful.

In those cases where the decrease of temperature of this embodimentalone fails to entrain the cardiac tissue, an alternative embodimentcomprises both a cooling element in the form of a contact device andmore conventional cardiac stimulation elements that apply an electricalpulse to the cardiac tissue in the form of a negative phase, as ananodal pulse followed by a negative pulse, or other stimulation methodknown in the art.

This combination of cooling of cardiac tissue combined with cardiacstimulation comprises yet another embodiment of the present invention. Aprocessor in the implantable device senses the onset of fibrillation andfirst applies cold temperature to the cardiac tissue. If this fails toaffect the reentry circuits of the heart, a combination of cooling andelectrical stimulation and/or electrical stimulation alone could then beapplied. If the combination does not affect the reentry circuit, thenindividual pacing in the more conventional fashion could be applied.Thus sensing and the application of stimulation of either coldtemperature electrical stimulation or a combination thereof are providedby circuitry within the implantable device.

The application of the embodiments described above would not requireanesthesia and would potentially have a higher effective rate thanconventional cardio-version.

A further embodiment of the present invention involves connecting theimplantable device to a communication terminal, preferably wireless, sothat an appropriate caregiver can receive notice of a cardiac event.Signals could then be received by the physician indicating thecondition. The physician would then have the option to remotely controlthe stimulation protocol applied by the implantable device of thepresent invention.

Yet another embodiment of the present invention involves altering theconductance of the heart by application of cold temperature with otherforms of pacing such as rate control and defibrillation. Pacing includesbut is not limited to bipolar, biphasic, unipolar, monophasic,overdrive, atrial alone, atrio-ventricular and sequential pacing.

An embodiment of the present invention provides methods for inhibitingthe conduction of spurious electrical impulses in cardiac tissuecomprising establishing a temperature conducive to inhibited conductionof electrical impulses for a targeted portion of the heart and applyinga temperature decrease to the targeted portion to maintain theestablished temperature.

Another embodiment of the present invention provides methods forinhibiting the conduction of spurious electrical impulses in cardiactissue. The method comprising sensing the onset of arrhythmia,determining the temperature of the cardiac tissue at the time of onsetof arrhythmia, and applying a temperature decrease below the presenttemperature to the cardiac tissue.

Another embodiment of the present invention provides methods forinhibiting the conduction of spurious electrical impulses in cardiactissue. A heat-transfer operator is situated at each of one or moretargeted portions of the heart. In an embodiment of the presentinvention, the heat-transfer operator is a Peltier cooler. In anotherembodiment of the present invention, the heat-transfer operator is aheat sink that is thermally coupled to a Peltier cooler. A symptomassociated with an arrhythmia is detected, and, in response to detectionof the symptom, the heat is selectively transferred away from thetargeted portion in the heart related to arrhythmia by absorbing heatinto the heat-transfer operator situated at the targeted portion.

In another embodiment of the present invention, methods for suppressingarrhythmia in a patient are provided. A heat-transfer operator isimplanted at each of one or more targeted portions of a patient's heart.At least one heat-transfer operator is operated to cool at least onetargeted portion of the heart, thereby suppressing the arrhythmia.

In still another embodiment of the present invention, methods areprovided for inhibiting the conduction of spurious electrical impulsesin cardiac tissue. The onset of arrhythmia is sensed and the sensedarrhythmia evaluated. The temperature of the cardiac tissue at the timeof onset of arrhythmia is also determined. Based on the evaluation ofthe sensed arrhythmia and cardiac tissue temperature, one or moreremedial measures is selected from the group consisting of applying atemperature decrease to the cardiac tissue and applying a pacing pulseto the cardiac tissue. The selected remedial measure is applied.

Another embodiment of the present invention comprises apparatuses forinhibiting the conduction of spurious electrical impulses in cardiactissue. A sensing means senses the onset of arrhythmia. A cooling meansresponsive to the sensing means applies a cooling stimulus to thecardiac tissue. In yet another embodiment of the present invention,apparatuses are provided for inhibiting the conduction of spuriouselectrical impulses in cardiac tissue. A sensor detects a symptomassociated with an arrhythmia. A heat-transfer operator is situated ateach of one or more targeted portions of the heart. In an embodiment ofthe present invention, the heat-transfer operator is a Peltier cooler.In another embodiment of the present invention, the heat-transferoperator is a heat sink coupled to a Peltier cooler implanted in thetorso of the patient. The heat-transfer operator at each of the one ormore targeted portions is adapted to respond to the sensor to removeheat from the targeted portion served by that heat-transfer operator.

In still another embodiment of the present invention, apparatuses forsuppressing arrhythmia in a patient are provided. A sensor detects asymptom associated with an arrhythmia. A heat-transfer operator isimplanted at each of one or more targeted portions of a patient's heart.In response to the detection of arrhythmia, the heat-transfer operatorat each of the one or more targeted portions is adapted to transfer heataway from the targeted portion served by that heat-transfer operatorsuch that each of the one or more targeted portions is cooled and thearrhythmia is suppressed.

BRIEF DESCRIPTION OF THE DRAWINGS

FIG. 1 illustrates a methodology for inhibiting the conduction ofspurious electrical impulses in cardiac tissue according to embodimentsof the present invention

FIG. 2 illustrates a methodology for inhibiting the conduction ofspurious electrical impulses in cardiac tissue by application of atemperature decrease to cardiac tissue according to embodiments of thepresent invention.

FIG. 3 illustrates a methodology for inhibiting the conduction ofspurious electrical impulses in cardiac tissue by application of atemperature decrease and at least one pacing pulse to cardiac tissueaccording to embodiments of the present invention.

FIG. 4 illustrates a methodology for suppressing arrhythmia by selectiveapplication of a temperature decrease to a targeted portion of the heartand pacing pulses to cardiac tissue according to embodiments of thepresent invention.

FIG. 5 illustrates an apparatus for inhibiting the conduction ofelectrical impulses in cardiac tissue by application of a temperaturedecrease to a targeted portion of the heart according to embodiments ofthe present invention.

DETAILED DESCRIPTION

Embodiments of the present invention provide systems and methods fortreating cardiac tissue by cooling the cardiac tissue to inhibit theconduction of certain electrical signals in cardiac tissue and decreasethe duration of tachycardia and enhance the effects of pacing anddefibrillation stimuli. In the description of these embodiments,reference is made to sensing a “symptom” indicative of a condition ofthe heart that may be treated by application of the present invention.For the purpose of the present invention, the term “symptom” is usedbroadly to encompass any sign or indication of such a condition that canbe detected through direct or indirect sensing of physiologicalparameters.

An embodiment of the present invention comprises an implantable cardiactreatment/stimulation device designed to inhibit the conduction ofspurious electrical signals in cardiac tissue without pacing. Thetechnique applied in the implantable device comprises a cooling elementfor cooling cardiac tissue. Optionally, one or both of the coolingembodiments may be provided in combination with cathodal-only orbiphasic stimulation of the cardiac tissue.

An embodiment of the present invention provides a method for inhibitingthe conduction of spurious electrical impulses in cardiac tissue. Themethod comprises establishing a temperature conducive to inhibitedconduction of electrical impulses for a targeted portion of the heart;and applying a temperature decrease to the targeted portion to maintainthe established temperature. The temperature of the targeted portion issensed. If the targeted portion has reached the established temperature,the application of the temperature decrease is ceased. If the targetedportion has not achieved the established temperature, application of thetemperature decrease to the targeted portion continues.

The decrease in temperature of the cardiac tissue may be achievedthrough various means, including by way of example and not as alimitation, applying a cooling fluid to the cardiac tissue, electricallycooling the cardiac tissue, and mechanically cooling the cardiac tissue.

Another embodiment of the present invention provides methods forinhibiting the conduction of spurious electrical impulses in cardiactissue. The method comprises sensing the onset of arrhythmia,determining the temperature of the cardiac tissue at the time of onsetof arrhythmia, and applying a temperature decrease to the cardiactissue. In another method, the functioning of the cardiac tissue issensed. If the cardiac tissue reverts to sinus rhythm, the applicationof the temperature decrease is ceased. If the cardiac tissue has notreverted to sinus rhythm, the application of the temperature decrease tothe cardiac tissue is continued.

The decrease in temperature of the cardiac tissue may be achievedthrough various means, including by way of example and not as alimitation, applying a cooling fluid to the cardiac tissue, electricallycooling the cardiac tissue, mechanically cooling the cardiac tissue, andcooling the cardiac tissue via an endothermic chemical reaction.Examples of cooling devices suitable for use in practicing the presentinvention are evaporative coolers, radiative coolers, chillers, thermalholdover devices (such as thermal storage units, with or withoututilization of phase change phenomena), and gas expansion coolers.Cooling may be accomplished via a heat exchanger structure or via directcontact.

In another embodiment of the present invention, sensing the onset ofarrhythmia comprises sensing a symptom indicative of arrhythmia. Varioussymptoms indicative of arrhythmia may be sensed, including by way ofexample and not as a limitation, an electrical change within the heart,and a change in a measure of heart function.

In another embodiment of the present invention, a method for inhibitingthe conduction of spurious electrical impulses in cardiac tissue furthercomprising applying a pacing pulse to cardiac tissue. Pacing may beaccomplished by one or more electrodes in contact with cardiac tissue,or electrodes located in the blood pool of one or more of the heartchambers. In either method, the pacing pulse is applied to the one ormore electrodes. The pacing pulse may be a cathodal electrical waveformor a biphasic electrical waveform comprising cathodal and anodalelements.

Another embodiment of the present invention provides methods forinhibiting the conduction of spurious electrical impulses in cardiactissue. One or more portions of the heart affected by one or morereentry circuits is targeted. In an embodiment of the present invention,each of the one or more targeted portions is selected from the groupconsisting of a right anterior-lateral atrial surface, a leftanterior-lateral atrial surface, a right postero-lateral atrial surface,and a left postero-lateral atrial surface. A heat-transfer operator issituated at each of one or more targeted portions of the heart. In anembodiment of the present invention, the heat-transfer operator is aPeltier cooler. The Peltier cooler may be electrically connected to apower source implanted in the patient's torso. In another embodiment ofthe present invention, the heat-transfer operator is a heat sink that isthermally coupled to a Peltier cooler implanted in a patient's torso.Optionally, the heat sink is thermally coupled using a mechanicalcontact or a thermal transfer fluid.

A symptom associated with an arrhythmia is detected, and, in response todetection of the symptom, the heat is selectively transferred away fromthe targeted portion in the heart related to arrhythmia by absorbingheat into the heat-transfer operator situated at the targeted portion.

The symptom may be detected within the heart. The heat-transfer operatoris activated in response to the detection of arrhythmia. Varioussymptoms may be detected, including by way of example and not as alimitation, an electrical change within the heart and a change in ameasure of heart function.

Another method comprises sensing the functioning of the heart and, inthe event the symptom associated with arrhythmia is not detected,ceasing transferring heat away from at least one of the targetedportions.

In another embodiment of the present invention, a method for inhibitingthe conduction of spurious electrical impulses in cardiac tissue furthercomprising applying a pacing pulse to cardiac tissue. Pacing may beaccomplished by one or more electrodes in contact with cardiac tissue,or electrodes located in the blood pool of one or more of the heartchambers. In either method, the pacing pulse is applied to the one ormore electrodes. The pacing pulse may be a cathodal electrical waveformor a biphasic electrical waveform comprising cathodal and anodalelements.

In another embodiment of the present invention, a method for inhibitingthe conduction of spurious electrical impulses in cardiac tissuecomprises applying a pacing pulse to cardiac tissue. Pacing may beaccomplished by one or more electrodes in contact with cardiac tissue,or electrodes located in the blood pool of one or more of the heartchambers. In either method, the pacing pulse is applied to the one ormore electrodes. The pacing pulse may be a cathodal electrical waveformor a biphasic electrical waveform comprising cathodal and anodalelements.

In another exemplary embodiment of the present invention, a method forsuppressing arrhythmia in a patient is provided. A heat-transferoperator is implanted at each of one or more targeted portions of apatient's heart. At least one heat-transfer operator is operated to coolat least one targeted portion of the heart, thereby suppressing thearrhythmia. In an embodiment of the present invention, the heat-transferoperator is a Peltier cooler implanted on one or more targeted portions,each selected from the group consisting of a right anterior-lateralatrial surface, a left anterior-lateral atrial surface, a rightpostero-lateral atrial surface, and a left postero-lateral atrialsurface. The Peltier cooler may be electrically connected to a powersource implanted in the patient's torso. In another embodiment of thepresent invention, the heat-transfer operator is a heat sink implantedon one or more targeted portions each selected from the group consistingof a right anterior-lateral atrial surface, a left anterior-lateralatrial surface, a right postero-lateral atrial surface, and a leftpostero-lateral atrial surface that is thermally coupled to a Peltiercooler implanted in a patient's torso. Optionally, the heat sink isthermally coupled using a mechanical contact or a thermal transferfluid.

Another method for suppressing arrhythmia in a patient comprisesimplanting in the patient's heart at least one sensing-contact forsensing a symptom and connecting the sensing-contact to a power sourcethat supplies power for the operation of the heat-transfer operator uponthe sensing of a symptom. Various symptoms may be sensed, including byway of illustration and not as a limitation, an electrical change withinthe heart, and a measure of heart function.

In another embodiment of the present invention, the method forsuppressing arrhythmia in a patient further comprises applying a pacingpulse to cardiac tissue. Pacing may be accomplished by one or moreelectrodes in contact with cardiac tissue, or electrodes located in theblood pool of one or more of the heart chambers. In either method, thepacing pulse is applied to the one or more electrodes. The pacing pulsemay be a cathodal electrical waveform or a biphasic electrical waveformcomprising cathodal and anodal elements.

In still another embodiment of the present invention, methods areprovided for inhibiting the conduction of spurious electrical impulsesin cardiac tissue. The onset of arrhythmia is sensed and the sensedarrhythmia evaluated. The temperature of the cardiac tissue at the timeof onset of arrhythmia is also determined. Based on the evaluation ofthe sensed arrhythmia and cardiac tissue temperature, one or moreremedial measures is selected from the group consisting of applying atemperature decrease to the cardiac tissue and applying a pacing pulseto the cardiac tissue. The selected remedial measure is applied.Optionally, the cardiac tissue function is sensed, and if the cardiactissue reverts to sinus rhythm, the application of the remedial measureceases. Similarly, if the cardiac tissue does not revert to sinusrhythm, application of the remedial measure continues.

In still other embodiments of the present invention, apparatuses forinhibiting the conduction of spurious electrical impulses in cardiactissue are provided. An apparatus comprises a sensing means for sensingthe onset of arrhythmia and a cooling means responsive to the sensingmeans for applying a cooling stimulus to the cardiac tissue. Anapparatus further comprises logic means for sensing when a sinus rhythmhas been reestablished in the cardiac tissue and for halting the coolingstimulus in the event a sinus rhythm has been reestablished. Additionalmeans are provided to continue the cooling stimulus in the event a sinusrhythm has not been reestablished.

Cooling means include, by way of illustration and not as a limitation,means for applying a cooling fluid to the cardiac tissue, an electricalcooling apparatus, and a mechanical cooling apparatus. Additionally, thesensing means may be adapted to sense a symptom associated with anarrhythmia. By way of illustration and not as a limitation, the symptommay be an electrical change within the heart and a measure of heartfunction.

Another apparatus of the present invention further comprises a cardiacstimulation generator and one or more electrodes in contact with cardiactissue. The electrodes are connected to the cardiac stimulationgenerator, which is adapted to apply a pacing pulse as a cathodalelectrical waveform or a biphasic waveform to the cardiac tissue. In analternative embodiment of the present invention, the electrodes are incontact with the cardiac blood pool. Optionally, the cardiac stimulationgenerator is responsive to the sensing means.

Yet another apparatus of the present invention for inhibiting theconduction of spurious electrical impulses in cardiac tissue comprises asensor for detecting a symptom associated with an arrhythmia. By way ofillustration and not as a limitation, the symptom may be an electricalchange within the heart, a measure of heart function, and a changeindicative of an arrhythmia. A heat-transfer operator is situated ateach of one or more targeted portions in the heart. In an embodiment ofthe present invention, the heat-transfer operator is a Peltier cooler.The Peltier cooler may be electrically connected to a power sourceimplanted in the patient's torso. In another embodiment of the presentinvention, the heat-transfer operator is a heat sink that is thermallycoupled to a Peltier cooler implanted in a patient's torso. Optionally,the heat sink is thermally coupled using a mechanical contact or athermal transfer fluid.

The heat-transfer operator at each of the one or more targeted portionsis adapted to respond to the sensor to remove heat from the targetedportion served by that heat-transfer operator. The sensor may be locatedon the heat-transfer operator.

An apparatus further comprises logic means for sensing when a sinusrhythm has been reestablished in the cardiac tissue and for halting thecooling stimulus in the event a sinus rhythm has been reestablished.Additional means are provided to continue the cooling stimulus in theevent a sinus rhythm has not been reestablished.

In another embodiment of the present invention, the apparatus furthercomprises a power source adapted to apply power to the sensor and toactivate the heat-transfer operator upon detection of a symptom.Optionally, the power source stores sufficient energy to suppressarrhythmia in a patient for an extended period of time. Additionally,the power source automatically ceases to apply power to theheat-transfer operator after the one or more targeted portions aresufficiently cooled. In an embodiment of the present invention, the oneor more targeted portions are sufficiently cooled when there is asubsidence of the symptom as detected by the sensing-contact.Alternatively, the one or more targeted portions are sufficiently cooledwhen each targeted portion reaches a predetermined temperature asmeasured by a thermacouple. In yet another alternative embodiment, theone or more targeted portions are sufficiently cooled when heat istransferred away from the one or more targeted portions for a programmedperiod of time.

In an embodiment of the present invention, each of the one or moretargeted portions is selected from the group consisting of a rightanterior-lateral atrial surface, a left anterior-lateral atrial surface,a right postero-lateral atrial surface, and a left postero-lateralatrial surface.

In another embodiment of the present invention, the apparatus furthercomprises a cardiac stimulation generator and one or more electrodes incontact with cardiac tissue. The electrodes are connected to the cardiacstimulation generator, which is adapted to apply a pacing pulse as acathodal electrical waveform or a biphasic waveform to the cardiactissue. In an alternative embodiment of the present invention, theelectrodes are in contact with the cardiac blood pool. Optionally, thecardiac stimulation generator is responsive to the sensing means.

Yet another apparatus of the present invention suppresses arrhythmia ina patient. The apparatus comprises a sensor for detecting a symptomassociated with an arrhythmia. By way of illustration and not as alimitation, the symptom may be an electrical change within the heart, ameasure of heart function, and a change indicative of an arrhythmia. Aheat-transfer operator is situated at each of one or more targetedportions in the heart, In response to the detection of arrhythmia, theheat-transfer operator at each of the one or more targeted portions isadapted to transfer heat away from the targeted portion served by thatheat-transfer operator. As result, each of the one or more targetedportions is cooled, and the arrhythmia is suppressed.

In an embodiment of the present invention, the heat-transfer operator isa Peltier cooler. The Peltier cooler may be electrically connected to apower source implanted in the patient's torso. The power source isadapted to apply power to the sensor and to activate the heat-transferoperator upon the detection of a symptom. In another embodiment of thepresent invention, the heat-transfer operator is a heat sink that isthermally coupled to a Peltier cooler implanted in a patient's torso.Optionally, the heat sink is thermally coupled using a mechanicalcontact or a thermal transfer fluid.

In yet another embodiment of the present invention, the one or moretargeted portions is each selected from the group consisting of a rightanterior-lateral atrial surface, a left anterior-lateral atrial surface,a right postero-lateral atrial surface, and a left postero-lateralatrial surface.

In another embodiment of the present invention, the apparatus furthercomprises a power source adapted to apply power to the sensor and toactivate the heat-transfer operator upon detection of a symptom.

In another embodiment of present invention, the apparatus furthercomprises a cardiac stimulation generator and one or more electrodes incontact with cardiac tissue. The electrodes are connected to the cardiacstimulation generator, which is adapted to apply a pacing pulse as acathodal electrical waveform or a biphasic waveform to the cardiactissue. In an alternative embodiment of the present invention, theelectrodes are in contact with the cardiac blood pool. Optionally, thecardiac stimulation generator is responsive to the sensor.

FIG. 1 illustrates a methodology for inhibiting the conduction ofspurious electrical impulses in cardiac tissue according to embodimentsof the present invention. Referring to FIG. 1, a temperature conduciveto inhibited conduction of electrical impulses is established for atargeted portion of the heart 100. A temperature decrease is applied tothe targeted portion to maintain the established temperature 110. Thetemperature of the targeted portion is sensed 115 and a determination ismade as to whether the targeted portion has reached the establishedtemperature 120. If the targeted portion has reached the establishedtemperature, the application of the temperature decrease is ceased 125.If the targeted portion has not achieved the established temperature,application of the temperature decrease to the targeted portioncontinues 130. While FIG. 1 illustrates a single targeted portion, thepresent invention is not so limited. One or more targeted portions maybe identified and associated with an established temperature 120 withoutdeparting from the scope of the present invention.

The decrease in temperature of the cardiac tissue may be achievedthrough various means, including by way of example and not as alimitation, applying a cooling fluid to the cardiac tissue, electricallycooling the cardiac tissue, and mechanically cooling the cardiac tissue.

FIG. 2 illustrates a methodology for inhibiting the conduction ofspurious electrical impulses in cardiac tissue by application of atemperature decrease to cardiac tissue according to embodiments of thepresent invention. Referring to FIG. 2, the onset of arrhythmia issensed 200 and a temperature decrease applied to cardiac tissue 210. Thefunctioning of the cardiac tissue is sensed 215 and a determination ismade as to whether the cardiac tissue has reverted to sinus rhythm 220.If the cardiac tissue has reverted to sinus rhythm, the application of atemperature decrease to the cardiac tissue is ceased 225. If the cardiactissue has not reverted to sinus rhythm, the application of atemperature decrease to the cardiac tissue is continued 230.

FIG. 3 illustrates a methodology for inhibiting the conduction ofspurious electrical impulses in cardiac tissue by application of atemperature decrease and at least one pacing pulse to cardiac tissueaccording to embodiments of the present invention. Referring to FIG. 3,the onset of arrhythmia is sensed 300. At least one pacing pulse and atemperature decrease are applied to cardiac tissue 310. The functioningof the cardiac tissue is sensed 315 and a determination is made as towhether the cardiac tissue has reverted to sinus rhythm 320. If thecardiac tissue has reverted to sinus rhythm, the application of the atleast one pacing pulse and a temperature decrease to the cardiac tissueis ceased 325. If the cardiac tissue has not reverted to sinus rhythm,the application of the at least one pacing pulse and a temperaturedecrease is continued 330. As previously described, a pacing pulse maybe cathodal or biphasic and may be applied to the cardiac tissue throughelectrodes in contact with the blood pool of the heart or in contactwith the cardiac tissue.

FIG. 4 illustrates a methodology for suppressing arrhythmia by selectiveapplication of a temperature decrease to a targeted portion of the heartand pacing pulses to cardiac tissue according to embodiments of thepresent invention. Referring to FIG. 4, the onset of arrhythmia issensed 400. The arrhythmia is evaluated and the temperature of thecardiac tissue is determined 405. Based on the evaluation of the sensedarrhythmia and cardiac tissue temperature, one or more remedial measuresis selected from the group consisting of applying a temperature decreaseto the cardiac tissue and applying a pacing pulse to the cardiac tissue410. The selected remedial measure(s) is (are) applied to the cardiactissue 415. The selective application of heart cooling and pacing pulsesis determined by logic incorporated into a computer processor. In anembodiment of the present invention, the processor is located in themeans that provides the pacing pulse. Alternatively, the processor islocated in the means that provides the cooling function. In yet anotherembodiment of the present invention, the processor is a separate device.The functioning of the cardiac tissue is sensed 420 and a determinationis made as to whether the cardiac tissue has reverted to sinus rhythm425. If the cardiac tissue has reverted to sinus rhythm, the applicationof the selected remedial measure(s) ceases 430. If the cardiac tissuehas not reverted to sinus rhythm, the application of the selectedremedial measure(s) continues 435. In an alternate embodiment, thetemperature of the cardiac tissue and the arrhythmia are re-evaluatedand one or more remedial measures are again selected.

As previously described, the pacing pulse may be cathodal or biphasicand may be applied to the cardiac tissue through electrodes in contactwith the blood pool of the heart or in contact with the cardiac tissue.

FIG. 5 illustrates an apparatus for inhibiting the conduction ofspurious electrical impulses in cardiac tissue by application of atemperature decrease to a targeted portion of the heart according toembodiments of the present invention. Referring to FIG. 5, a heartsensing means 510 and a heart cooling means 515 are applied to a heart505 in a patient 500. In an embodiment of the present invention, heartsensing means 510 senses the onset of arrhythmia. In response to theheart sensing means 510, cooling is applied to the heart via heartcooling means 515. Logic 520 senses when a sinus rhythm has beenreestablished in the cardiac tissue. If a sinus rhythm has beenreestablished in the cardiac tissue, logic 520 halts the coolingstimulus to cooling means 515. If a sinus rhythm has not beenreestablished in the cardiac tissue, logic 520 continues the coolingstimulus to cooling means 515.

In an embodiment of the present invention, heart cooling means 515comprises a Peltier cooler. Such heat-transfer operators passelectricity through junctions between dissimilar metals. The atoms ofthe dissimilar metals have a difference in energy levels that results ina step between energy levels at each of the junctions. As electricity ispassed through the metals, the electrons of the metal with the lowerenergy level pass the first step as they flow to the metal with thehigher energy level. In order to pass this step and continue thecircuit, the electrons must absorb heat energy that causes the metal atthe first junction to cool. At the opposite junction, where electronstravel from a high energy level to a low energy level they give offenergy which results in an increase in temperature at that junction.

As will be appreciated by those skilled in the art, other cooling meansmay be utilized to perform the functions of the present inventionwithout departing from its scope. By way of illustration and not as alimitation, heart cooling means 515 may be another device or system thatabsorbs heat from a specific area and accomplishes heat transfer throughconvection of fluids or conduction. Alternatively, cooling may beaccomplished by a mechanical hydraulic system for pumping cooled fluidinto a bladder on the surface of the atrium. The amount of coolingapplied and the total temperature of the heart may be monitored througha “thermostat” function of the apparatus.

In another embodiment of the present invention, heart cooling meansfurther comprises a heat sink thermally coupled to a heat-transferoperator, such as a Peltier cooler. The heat-transfer operator iselectrically connected to a power source that supplies a current throughthe heat-transfer operator to affect heat transfer. The power sourceoperates efficiently by powering off the heat-transfer operator supplywhen heat transfer is not needed. When heat transfer is desired, thepower source can be activated to supply a DC current to theheat-transfer operator that will, in turn, activate heat transfer fromthe targeted portion through the temperature-contact to the coldjunction of the heat-transfer operator.

In another embodiment of the present invention, the heat-transferoperator is responsive to the heart sensing means 510, which detects asymptom of arrhythmia. The symptoms detected by the heart sensing meansmay be electrical or physiological measures indicative of arrhythmia.

In yet another embodiment of the present invention, logic 520 determinesa time for sufficiently cooling the heart. The time necessary forsufficient cooling may be programmed into logic 520 or may be calculatedby logic 520 based on information obtained from heart sensing means 510.

Referring again to FIG. 5, in another embodiment of the presentinvention, a cardiac stimulation generator 530 applies a pacing pulse tothe cardiac tissue via electrode 525. While FIG. 5 illustrates a singleelectrode, the present invention is not so limited. As will beappreciated by those skilled in the art, multiple electrodes may beutilized without departing from the scope of the present invention.Additionally, electrode 525 may be placed in contact with the cardiactissue or be located within a blood pool of the heart. Cardiacstimulation generator 530 is responsive to heart sensing means 510. Thepacing pulse generated by cardiac stimulation generator 530 may be acathodal electrical waveform or a biphasic electrical waveformcomprising cathodal and anodal elements.

While the embodiments of the present invention have been directed tocooling cardiac tissue for the purpose of inhibiting the conduction ofspurious electrical impulses, the present invention is not so limited.Spurious electrical signals affect other parts of the human body (e.g.,the brain, skeletal muscles, pain receptors) that can be inhibited bycooling. As would be apparent to those skilled in the art, theembodiments of the present invention may be applied to inhibit spuriouselectrical signals of other parts of the body without departing from thescope of the present invention.

Systems and methods for inhibiting the conduction of spurious electricalimpulses in cardiac tissue have been described. It will be understood bythose skilled in the art that the present invention may be embodied inother specific forms without departing from the scope of the inventiondisclosed and that the examples and embodiments described herein are inall respects illustrative and not restrictive. Those skilled in the artof the present invention will recognize that other embodiments using theconcepts described herein are also possible. Further, any reference toclaim elements in the singular, for example, using the articles “a,”“an,” or “the” is not to be construed as limiting the element to thesingular.

1. An apparatus for inhibiting the conduction of spurious electricalimpulses in cardiac tissue comprising: a cardiac sensor for detecting asymptom associated with an arrhythmia; a temperature sensor, wherein thetemperature sensor detects a start temperature of the cardiac tissue atthe time the symptom is detected; a processor comprising logic adaptedfor: evaluating the sensed arrhythmia and the cardiac tissue starttemperature; and using the evaluation of the sensed arrhythmia and thecardiac tissue temperature, selecting one or more remedial measures fromthe group consisting of applying a temperature decrease to the cardiactissue and applying a pacing pulse to the cardiac tissue; aheat-transfer operator situated at a targeted portion, wherein the heattransfer operator is adapted to respond to the processor to remove heatfrom the targeted portion served by that heat-transfer operator if thetemperature decrease remedial measure is selected; a cardiac stimulationgenerator; and a cardiac stimulation electrode, wherein the electrode isconnected to the cardiac stimulation generator, and wherein the cardiacstimulation generator is adapted to apply a pacing pulse to the cardiactissue if the pacing pulse remedial measure is selected.
 2. Theapparatus of claim 1, wherein the heat-transfer operator is selectedfrom the group consisting of a means for applying a cooling fluid to thecardiac tissue, an electrical cooling apparatus, a mechanical coolingapparatus, and an endothermic chemical reaction.
 3. The apparatus ofclaim 1, wherein the heat-transfer operator is a Peltier cooler.
 4. Theapparatus of claim 3, wherein the heat-transfer operator comprises aheat sink thermally coupled to a Peltier cooler enclosed in a housingthat is implanted in the patient's torso.
 5. The apparatus of claim 4,wherein the heat sink is coupled to the Peltier cooler throughmechanical contact.
 6. The apparatus of claim 4, wherein the heat sinkis coupled to the Peltier cooler through a thermal transfer fluid. 7.The apparatus of claim 4, wherein the Peltier cooler is electricallyconnected to a power source located within the housing.
 8. The apparatusof claim 1, wherein the cardiac stimulation electrode is planted in thecardiac tissue.
 9. The apparatus of claim 1, wherein the cardiacstimulation electrode is placed in contact with a cardiac blood pool andthe pacing pulse is applied to the cardiac tissue through the cardiacblood pool.
 10. The apparatus of claim 1, wherein the pacing pulse is acathodal electrical waveform.
 11. The apparatus of claim 1, wherein thepacing pulse is a biphasic electrical waveform.
 12. The apparatus ofclaim 1, wherein the temperature sensor further measures a currenttemperature of the cardiac tissue and wherein the processor furthercomprises logic for: monitoring the current temperature of the cardiactissue as determined by the temperature sensor; and ceasing thetemperature decrease remedial when the current temperature is less thanor equal to a desired temperature.